Hradilek A, Neuwirt J
Br J Haematol. 1986 Jan;62(1):21-30. doi: 10.1111/j.1365-2141.1986.tb02896.x.
The ability of seven monoclonal antibodies (MAbs) reactive with human transferrin (Tf) to inhibit iron uptake from Tf by cells of the human lymphoid line MOLT 3 was compared with the effect of these MAbs on Tf binding to MOLT 3 surface Tf receptors. MAbs HTF-01, HTF-06, HTF-07, HTF-11 and HTF-14 inhibited both iron uptake and Tf binding. Complexing Tf with MAbs HTF-04 or HTF-05 resulted in an increased association of Tf with the cells but iron uptake was diminished. Following the intracellular kinetics of Tf/HTF-04 complex has shown that the whole complex is endocytosed and Tf iron is retained inside the cell, but Tf release from both the cell surface and the intracellular compartment is slower when compared to Tf alone. Iron uptake inhibition was therefore attributed to lengthening of the Tf cell cycle after complexing of Tf with HTF-04 and it is suggested that the rate of cellular Tf turnover might, together with the number of functioning Tf receptors, determine the rate of iron uptake by cells.
将七种与人转铁蛋白(Tf)反应的单克隆抗体(MAb)抑制人淋巴系MOLT 3细胞从Tf摄取铁的能力,与这些MAb对Tf结合MOLT 3表面Tf受体的影响进行了比较。单克隆抗体HTF-01、HTF-06、HTF-07、HTF-11和HTF-14既抑制铁摄取也抑制Tf结合。Tf与单克隆抗体HTF-04或HTF-05复合导致Tf与细胞的结合增加,但铁摄取减少。追踪Tf/HTF-04复合物的细胞内动力学表明,整个复合物被内吞,Tf铁保留在细胞内,但与单独的Tf相比,Tf从细胞表面和细胞内区室的释放较慢。因此,铁摄取抑制归因于Tf与HTF-04复合后Tf细胞周期的延长,并且表明细胞Tf周转速率可能与功能性Tf受体的数量一起决定细胞摄取铁的速率。